Epigallocatechin-3-gallate (EGCG) has antibacterial, anti-inflammatory, antitumor, and other functions. EGCG and its anticancer mechanism are hot research topics in the prevention and treatment of oral cancer. In this paper, the prevention and treatment effects of EGCG on oral cancer and its anticancer mechanism are reviewed. The results show that EGCG can regulate multiple cell metabolic signaling pathways, such as the G protein coupled receptor signaling pathway, mitogen-activated protein kinase (MAPK), and the Wnt signaling pathway, and it can regulate DNA methylation and act on RNA of oral cancer cells directly or indirectly through the oral cancer cell signal transduction network to inhibit the development of oral precancerous lesions and oral cancer. EGCG combined with 5-fluorouracil can enhance the curative effect and reduce adverse effects and is expected to be a new drug for the prevention and treatment of oral cancer.

Eutrophils are the first innate immune cells to reach the site of inflammation. Neutrophils produce neutrophil extracellular traps (NETs) that can quickly capture and limit the spread of pathogens, facilitating the removal of pathogens and their debris. Neutrophils in the oral cavity are specifically transformed from circulating neutrophils in the blood, and the number of NETs released by oral neutrophils is much higher than that of circulating neutrophils, thus better maintaining the balance of the oral microenvironment. As a bimorphic fungus, only the mycelium phase of Candida albicans can induce NETs, which is related to the neutrophils' ability to sense the size of pathogenic microorganisms through neutrophil elastase. However, spherical Staphylococcus aureus are much smaller than Candida albicans, and they can still induce NETs. Porphyromonas gingivalis, as one of the microorganisms in the periodontitis complex, induces fewer NETs than Streptococcus oralis and Actinomycetes, which are two common oral microorganisms, and there may be a mechanism allowing them to escape neutrophilic immunity in the early stage of periodontitis. Although the two main pathways of NET production have been studied in detail, the mechanisms involved in the induction of NETs by different microorganisms, especially from oral neutrophils, are not well understood. This review describes the mechanism of the immune effects of pathogenic microorganisms on neutrophil NETs in the oral cavity, providing a reference for the search for therapeutic targets and the development of key drugs for treating oral infectious diseases.